Case study acute renal failure
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Case study: acute renal failure. Bruce R. Wall, MD, FACP 4/3/06 Renal resident conference. Patient P B. 80 yo white female with history of HBP for 20 years, and previous Left hemispheric CVA CC: “Doc, I was playing bridge 2 weeks ago…”

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Case study: acute renal failure

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Case study acute renal failure

Case study: acute renal failure

Bruce R. Wall, MD, FACP

4/3/06

Renal resident conference


Patient p b

Patient P B

  • 80 yo white female with history of HBP for 20 years, and previous Left hemispheric CVA

  • CC: “Doc, I was playing bridge 2 weeks ago…”

  • Known lumbosacral spine stenosis/listhesis with increasing back pain and loss of strength in lower legs

  • 1 week of nausea and vomiting with minimal abd pain

  • Two year history of ibuprofen use; recent conversion of naprosyn for 1 month…

  • No abd distension; no hematemesis; occasional pink tinged sputum, while on Plavix

  • Conversion to Ultram, then narcotics, which caused constipation


H p continued

H & P continued

  • No previous documentation of creat in caregate; current creat 2.5 to 3.5mg%

  • Iron deficiency anemia documented; negative colonscopy 1 year ago

  • GI consulted for nausea, vomiting, anemia after naprosyn exposure; EGD WNL

  • Renal consulted for ARF? CRF?

  • Lower leg weakness, poor gait, and GI symptoms were her main concerns


Past history

PAST HISTORY

  • Hypertension 20 yrs

  • Coronary artery stent 2002

  • CVA with mild expressive aphasia

  • Anemia

  • CKD

  • Diverticulae and internal hemorrhoids

  • Lumbar stenosis, moderate, at L3-4

  • Cholecystectomy, appy, & TAH


History continued

History: continued

  • FH: HBP, CVA & ASCVD at young age

  • SH: remote smoker, very active, no ETOH

  • ROS: ataxia with abnormal gait, requiring walker; GI symptoms; no history of CHF; no nephrolithiais, no endocrinopathy, no diabetes; able to drive


Medications

Amitriptyline

Aspirin 81 mg

Atorvastatin

Clonidine TTS

Plavix

Iron

Lisinopril

Metoprolol

Protonix

Morphine

SL nitroglycerin

Vitamin K

Centrum

ALLERGY:Voltaren (nausea)

Medications:


Physical exam

Physical exam

  • 140/88 90 14 afebrile

  • Awake, alert, preserved muscle mass;

  • HEENT: minimal facial asymmetry

  • NECK: no nodes, chronic stiffness

  • LUNGS: no hemoptysis; no rales

  • COR: RRR, no murmur, no gallop

  • ABD: soft, benign, no hepatomegaly

  • GU: positive stool occult blood, no mass

  • EXT: impressive 3+ edema; no purple toes

  • NEURO: expressive aphasia; abnormal gait; no hyperreflexia


Laboratory exam

Laboratory exam

  • Hgb 9gms; normocytic; plts WNL

  • Serum iron 20, ferritin 325, sat 18%

  • Nomal LFT’s and normal coags

  • Sodium 128 Potassium 5.1 Chloride 100 BUN 34 creatinine 2.8 Glucose 100 bicarbonate 23 calcium 7.6 albumin 2.7 cholesterol 225


Labs continued

Labs: continued

  • CXR - borderline cardiomegaly

  • Urinalysis: yellow hazy SG 1.01 pH 5 large blood negative ketones RBC 25/HPF WBC 35/HPF 2+protein

  • Sonography: left 10.7cm, right 11.9cm “isoechoic with the liver”

  • 24 hour urine: clearance 9ml/min; total protein = 1100mg per day


Additional information

Additional information

  • Any additional history required?

  • Any additional physical exam?

  • Labs pending: repeat 24hr urine, complements, myeloma markers, lupus markers, vasculitis markers


Differential diagnosis

Differential diagnosis:

  • This slide intentionally left blank


Approach to kidney

Approach to kidney

  • Acute vs chronic disease

  • Nephritic vs nephrotic syndrome

  • Glomerular disease:acute vs chronic GN

  • Interstitial disease: infiltrative, AIN

  • Renal artery disease: stenosis or emboli

  • Obstructive disease: tubules, stones, retroperitoneum, BPH vs prostate CA


Don t fall in love with your first diagnosis

“don’t fall in love with your first diagnosis…”

TOXIC EFFECTS of NSAIDS –

GI toxicity – upper and lower

Modest worsening of chronic hypertension

ARF – 2 different types

CV effects – blocks beneficial effect ASA

Hepatic injury

Bone marrow toxicity – aplasia

Anti-platelet effect – stop 5 days prior to surgery

CNS changes – tinnitus

Skin - TEN


Nsaid induced renal failure

NSAID induced renal failure

  • Hemodynamic mediated ARF: not a concern in normal individuals; yet patients with underlying GN, CKD, or hypercalcemia all need prostacyclin and PGE2

  • Patients with increased vasoconstrictors AII or NE – “states of volume depletion” CHF, cirrhosis, & DM are at greatest risk


Nsaid induced arf

NSAID induced ARF

  • Inhibition of PG by any NSAID in state of vasoconstriction may lead to reversible renal insufficiency or ARF

  • Indocin, ibuprofen, and toradol most common causes

  • COX II inhibition “reported” cause ARF

  • Sulindac/clinoril less suppression & ARF


Ain allergic interstitial nephritis

AIN: allergic interstitial nephritis

  • Fenoprofen and Indocin relatively common cause hematuria, pyuria, proteinuria; yet the full blown syndrome of fever,rash, eosinophilia is extremely uncommon

  • Nephotic range proteinuria is reported

  • Biopsy is uncommon since pts improve

  • Prednisone not helpful (retrospective)


Lab profile

Lab profile


Renal biopsy

Renal biopsy

  • Indication

  • Risk

  • Solitary kidney?

  • Complications

  • Follow up monitoring


Additional serology

Additional serology

  • Anti GBM negative

  • ANA 1:40 speckled

  • P–ANCA 1:32 with positive MPO (Myeloperoxidase IgG) of 55 units


Biopsy

biopsy


Overview to classification of rpgn

Overview to classification of RPGN

  • RPGN is the syndrome; crescentic GN is the pathologic entitiy

  • Crescent formation is a nonspecific response to injury of glomerular capillary wall

  • >80% crescents present -- severe ARF

  • Types of crescentic GN: type I: anti-GBM diseasetype II: immune complex diseasetype III: pauci-immune disease

  • Pauci-immune present with necrotizing GN with few or no immune deposits by IF or EM. Majority of patients with renal-limited vasculitis are P-ANCA positive with 75% MPO positive.


Overview to classification of rpgn1

Overview to classification of RPGN


Spectrum of anca

Spectrum of ANCA

  • Described in 1982

  • Technical issues: indirect IF assay is more sensitive & ELIZA more specific

  • C-ANCA pattern staining is diffuse @ cytoplasm (most are PR3 positive)

  • P-ANCA stains around the nucleus, (most are MPO positive)


Clinical applications of anca

Clinical applications of ANCA

  • Is a positive result a “true positive?” Yes, if ELIZA (+), fairly good PPV.

  • Does (-)ANCA exclude ANCA vasculitis? No, since 40% test (-) in Wegener’s.

  • Does presence of (+)ANCA establish the diagnosis (no biopsy required)? No, tissue confirmation is standard.

  • Does rising ANCA titer correlate with flare? No, not a reliable indicator of disease.

  • Does persistant (-)ANCA mean quiescence? No


Disease associations

Disease associations

  • ANCA are associated with may cases of WG, MPA,Churg-Strauss syndrome, “renal-limited vasculitis” and certain drug-induce syndromes (PTU, hydralazine, minocycline)


Therapy

therapy

  • Initial dosing with 1000mg solumedrol for 3 days

  • Intravenous cyclophosphamide every month has less toxicity than PO

  • Once in remission, consider PO imuran, methotrexate, or ENBREL?


Lab profile1

Lab profile


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